{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T20:04:47Z","timestamp":1793217887361,"version":"4.5.0"},"reference-count":45,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2019,11,20]],"date-time":"2019-11-20T00:00:00Z","timestamp":1574208000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81270354"],"award-info":[{"award-number":["81270354"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81470420"],"award-info":[{"award-number":["81470420"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Excessive immune\u2010mediated inflammatory reaction plays a deleterious role in ventricular remodelling after myocardial infarction (MI). Interleukin (IL)\u201038 is a newly characterized cytokine of the IL\u20101 family and has been reported to exert a protective effect in some autoimmune diseases. However, its role in cardiac remodelling post\u2010MI remains unknown. In this study, we found that the expression of IL\u201038 was increased in infarcted heart after MI induced in C57BL\/6 mice by permanent ligation of the left anterior descending artery. In addition, our data showed that ventricular remodelling after MI was significantly ameliorated after recombinant IL\u201038 injection in mice. This amelioration was demonstrated by better cardiac function, restricted inflammatory response, attenuated myocardial injury and decreased myocardial fibrosis. Our results in vitro revealed that IL\u201038 affects the phenotype of dendritic cells (DCs) and IL\u201038 plus troponin I (TNI)\u2010treated tolerogenic DCs dampened adaptive immune response when co\u2010cultured with CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells. In conclusion, IL\u201038 plays a protective effect in ventricular remodelling post\u2010MI, one possibility by influencing DCs to attenuate inflammatory response. Therefore, targeting IL\u201038 may hold a new therapeutic potential in treating MI.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.14741","type":"journal-article","created":{"date-parts":[[2019,11,20]],"date-time":"2019-11-20T03:01:02Z","timestamp":1574218862000},"page":"371-384","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["Interleukin\u201038 alleviates cardiac remodelling after myocardial infarction"],"prefix":"10.1111","volume":"24","author":[{"given":"Yuzhen","family":"Wei","sequence":"first","affiliation":[{"name":"Institute of Cardiology Union Hospital TongJi Medical College Huahzong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yin","family":"Lan","sequence":"additional","affiliation":[{"name":"Institute of Cardiology Union Hospital TongJi Medical College Huahzong University of Science and Technology Wuhan 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